RETRACTED: Candesartan and glycyrrhizin ameliorate ischemic brain damage through downregulation of the TLR signaling cascade

Barakat, Waleed; Safwet, Nancy; El-Maraghy, Nabila N.; Zakaria, Mohamed

doi:10.1016/j.ejphar.2013.12.032

Cited by 66 publications

(51 citation statements)

References 46 publications

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“…P53 influenced the binding of NF-κB to p300 and blocked NF-κB-mediated survival signaling. P53 also transferred to mitochondria and caused the release of cytochrome C. Candesartan and glycyrrhizin [25] were proved to alleviate the Toll-like receptor (TLR) pathway after MCAO, including upregulation of TLR-2, TLR-4, Myd88, TRIF, IRF-3, and downregulation of TNF-α, IL-1β, IL-6, and NF-κB. A study [26] proposed that erbB receptors were upregulated in neurons, macrophages, and microglia after cerebral infarction, which might be related to neuroprotection and repair.…”

Section: Discussionmentioning

confidence: 99%

Plasma MicroRNA-16 Is a Biomarker for Diagnosis, Stratification, and Prognosis of Hyperacute Cerebral Infarction

Tian

Yang

et al. 2016

PLoS ONE

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Indices for the diagnosis of hyperacute cerebral infarction (HACI) and the prediction of prognosis are essential for timely and appropriate management. MicroRNAs (miRNAs) that regulate gene expression following stroke have potential use as prognostic markers of HACI. Here, we explored whether concentrations of circulating miRNAs correlate with clinical outcomes and thus form a system of stroke stratification. Plasma samples from patients with HACI (n = 7) and age-matched healthy volunteers (HVT, n = 4) were screened by microarray to find differentially expressed miRNAs, some of which were further verified by quantitative reverse transcription polymerase chain reaction (qRT-PCR) (HACI:HVT = 33:23). The target genes of the miRNAs with verified differential expression were investigated by GO and KEEG analyses. Using the TOAST (OCSP) criteria and the 3-month modified Rankin Score (mRS), relationships among the expression patterns of specific miRNAs, stroke stratification, and clinical prognosis were determined. The microarray analysis revealed 12 differentially expressed miRNAs. Among seven selected miRNAs verified with qRT-PCR, miR-16 expression in the HACI group was the most significantly different from the HVT group (P < 0.01). Bioinformatics analysis showed that the potential target genes of miR-16 were mainly involved in programmed cell death and the p53 signaling pathways. Receiver operating characteristic (ROC) analysis showed that the area under the curve (AUC) of miR-16 was 0.775 (sensitivity 69.7% and specificity 87%) and 0.952 (sensitivity 100% and specificity 91.3%) in overall patients and patients with large artery atherosclerosis (LAAS), respectively. Elevated miR-16 expression was associated with the stroke subtype of LAAS, total anterior circulation infarction, partial anterior circulation infarction, and poor prognosis (P < 0.05). A diagnostic method based on rapid measurement of plasma miR-16 has the potential to identify hyperacute cerebral infarction with LAAS with high sensitivity and specificity, which would inform and improve early treatment decisions and disease management.

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Section: Discussionmentioning

confidence: 99%

Plasma MicroRNA-16 Is a Biomarker for Diagnosis, Stratification, and Prognosis of Hyperacute Cerebral Infarction

Tian

Yang

et al. 2016

PLoS ONE

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“…The expression of TLR2 and TLR4 in microglia contributes to neuronal damage in cerebral ischemia-reperfusion injuries [21–23]. Moreover, accumulating evidence indicated that the effective suppression of TLR2 and TLR4 signaling pathways in microglia can provide neuroprotection [24–28]. …”

Section: Discussionmentioning

confidence: 99%

“…In response to DAMPs, which are released by necrotic cells, the signal transduction of TLR2 and TLR4 is induced through MyD88, resulting in the degradation of I κ B and the translocation of NF- κ B into the nucleus; this induces the production of proinflammatory cytokines such as IL-1 β , IL-6, and TNF- α [11, 20]. Several studies have reported the effective inhibition of TLR2 and TLR4 expression in different models that exhibited decreased NF- κ B activity and proinflammatory cytokine suppression corresponding with decreased tissue damage [24, 25, 27, 28]. …”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effect of Paeonol Mediates Anti‐Inflammation via Suppressing Toll‐Like Receptor 2 and Toll‐Like Receptor 4 Signaling Pathways in Cerebral Ischemia‐Reperfusion Injured Rats

Liao

Tsai²,

et al. 2016

Evidence-Based Complementary and Alternative Medicine

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Paeonol is a phenolic compound derived from Paeonia suffruticosa Andrews (MC) and P. lactiflora Pall (PL). Paeonol can reduce cerebral infarction volume and improve neurological deficits through antioxidative and anti-inflammatory effects. However, the anti-inflammatory pathway of paeonol remains unclear. This study investigated the relationship between anti-inflammatory responses of paeonol and signaling pathways of TLR2 and TLR4 in cerebral infarct. We established the cerebral ischemia-reperfusion model in Sprague Dawley rats by occluding right middle cerebral artery for 60 min, followed by reperfusion for 24 h. The neurological deficit score was examined, and the brains of the rats were removed for cerebral infarction volume and immunohistochemistry (IHC) analysis. The infarction volume and neurological deficits were lower in the paeonol group (pretreatment with paeonol; 20 mg/kg i.p.) than in the control group (without paeonol treatment). The IHC analysis revealed that the number of TLR2-, TLR4-, Iba1-, NF-κB- (P50-), and IL-1β-immunoreactive cells and TUNEL-positive cells was significantly lower in the paeonol group; however, the number of TNF-α-immunoreactive cells did not differ between the paeonol and control groups. The paeonol reveals some neuroprotective effects in the model of ischemia, which could be due to the reduction of many proinflammatory receptors/mediators, although the mechanisms are not clear.

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“…When TLR2 and TLR4 are not activated, MyD88, IL-IR relative kinase (IRAK) combined with MyD88 regulating protein-toll relevant protein. When TLR2 and TLR4 are activated, toll relevant protein separated with MyD88 and IRAK, and then the phosphorylation of IRAK will result in the transfer of NFkB into the nuclear, which further activate the expression of various inflammatory factors [15][16][17][18]. There was research which reported that miR-146a and miR-146b can targeted regulate and control the expression of TLR2 and TLR4 [19,20].…”

Section: Discussionmentioning

confidence: 99%

Research of expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction before and after the intervention of rosuvastatin

Zhu¹,

Hou²,

Sun³

et al. 2017

JAD

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RETRACTED: Candesartan and glycyrrhizin ameliorate ischemic brain damage through downregulation of the TLR signaling cascade

Cited by 66 publications

References 46 publications

Plasma MicroRNA-16 Is a Biomarker for Diagnosis, Stratification, and Prognosis of Hyperacute Cerebral Infarction

Plasma MicroRNA-16 Is a Biomarker for Diagnosis, Stratification, and Prognosis of Hyperacute Cerebral Infarction

Neuroprotective Effect of Paeonol Mediates Anti‐Inflammation via Suppressing Toll‐Like Receptor 2 and Toll‐Like Receptor 4 Signaling Pathways in Cerebral Ischemia‐Reperfusion Injured Rats

Research of expression quantity of serum miR-146a and miR-146b in patients with acute cerebral infarction before and after the intervention of rosuvastatin

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